The Physiologic Steps to Muscle Contraction
The sequence of events that result in the contraction of an individual muscle fiber begins with a signal—the neurotransmitter, ACh—from the motor neuron innervating that fiber. The local membrane of the fiber will depolarize as positively charged sodium ions (Na+) enter, triggering an action potential that spreads to the rest of the membrane will depolarize, including the T-tubules. This triggers the release of calcium ions (Ca++) from storage in the sarcoplasmic reticulum (SR). The Ca++ then initiates contraction, which is sustained by ATP.
For a contraction to occur there must first be a stimulation of the muscle in the form of an impulse (action potential) from a motor neuron (nerve that connects to muscle). Note that one motor neuron does not stimulate the entire muscle but only a number of muscle fibres within a muscle. The individual motor neuron plus the muscle fibres it stimulates, is called a motor unit. The motor end plate (also known as the neuromuscular junction) is the junction of the motor neurons axon and the muscle fibres it stimulates. When an impulse reaches the muscle fibres of a motor unit, it stimulates a reaction in each sarcomere between the actin and myosin filaments. This reaction results in the start of a contraction and the sliding filament theory. The reaction, created from the arrival of an impulse stimulates the 'heads' on the myosin filament to reach forward, attach to the actin filament and pull actin towards the centre of the sarcomere. This process occurs simultaneously in all sarcomeres, the end process of which is the shortening of all sarcomeres. Troponin is a complex of three proteins that are integral to muscle contraction. Troponin is attached to the protein tropomyosin within the actin filaments, as seen in the image below. When the muscle is relaxed tropomyosin blocks the attachment sites for the myosin cross bridges (heads), thus preventing contraction. When the muscle is stimulated to contract by the nerve impulse, calcium channels open in the sarcoplasmic reticulum (which is effectively a storage house for calcium within the muscle) and release calcium into the sarcoplasm (fluid within the muscle cell). Some of this calcium attaches to troponin which causes a change in the muscle cell that moves tropomyosin out of the way so the cross bridges can attach and produce muscle contraction. In the gym or during exercise virtually all muscular fatigue occurring is energy system fatigue. That is, the rate of work within the muscle can not be maintained because ATP (energy) can no longer be provided. Strength and hypertrophy (training to make muscles stronger or bigger) training are prime examples of the types of training that can cause muscle failure due to energy system fatigue.
The contractions of muscles that allow us to move would not appear without the work done by motor units. Sir Charles Sherrington made a great contribution to the study of a human body when he stated that people could move due to the action that occurs between a motor (efferent) neuron and muscle fibers and introduced the concept of a motor unit. The researcher assumed that “each muscle fiber receives innervation from only one motor neuron, and that the muscle fiber faithfully responds to every impulse of the motor neuron” (Floeter 1). Finally, the largest fast-glycolytic units with high myosin ATPase activity come (“Motor Units” par. 7). As a rule, the muscles include different types of motor units in various proportions depending on the individual’s genetics; the quadriceps, for example, has a relatively equal proportion of slow and fast units. In this way, the extraocular muscles are fast motor units, while postural muscles are slow ones. Of course, it is impossible just to memorize all the information about the motor units in the spare of the moment. Still, its constituents are rather easy to remember, as there are only two of them. The connection between size and types is also clear. If the constitutes are large, the motor unit is also large and fast. The contradiction can provide an example: the eyes and extraocular muscles are small, so the units are fast. If motor neurons and muscle fibers are small, the motor unit is small and slow. The back and postural muscles in it are big, so the units are slow. Dealing with slow and fast motor units, it is critical to remember two opposites, slow-oxidative and fast-glycolytic. The intermediate part will have the characteristics of both of them and can be easily recollected when combining the names of these two: fast (glycolytic) + (slow) oxidative = fast-oxidative.
Summing up, muscle contraction is described by the sliding filament model of contraction. ACh is the neurotransmitter that binds at the neuromuscular junction (NMJ) to trigger depolarization, and an action potential travels along the sarcolemma to trigger calcium release from SR. The actin sites are exposed after Ca++ enters the sarcoplasm from its SR storage to activate the troponin-tropomyosin complex so that the tropomyosin shifts away from the sites. The cross-bridging of myosin heads docking into actin-binding sites is followed by the “power stroke”—the sliding of the thin filaments by thick filaments. The power strokes are powered by ATP. Ultimately, the sarcomeres, myofibrils, and muscle fibers shorten to produce movement.
Floeter, Mary. Structure and Function of Muscle Fibers and Motor Units 2010. Web.
McDonnall, Daniel, Gregory Clark, and Richard Normann. “Selective Motor Unit Recruitment via Intrafascicular Multielectrode Stimulation.” Canadian Journal of Physiology and Pharmacology 82.8-9 (2004): 599-609. Print.
Motor Units. n.d. Web.